Seminars & Events
Monday, February 11, 2013: Dr. Daphne Soares (University of Maryland College Park) will speak on "The Sensory World of Cavefishes" at 4:45 pm in Goodpaster Hall 195.
Monday, March 4, 2013: Dr. Joe Cheer (University of Maryland Baltimore) will speak on "Endogenous Cannabinoids and the Pursuit of Reward" at 4:45 pm in Goodpaster Hall 195.
Friday, April 12, 2013: Dr. Jill McGaughy (University of New Hampshire) will speak on "The Role of Cortical Norepinephrine in the Ontogeny of Executive Function" at 3:00 pm in Schaefer Hall 106.
Dr. Erin Johnson '02 recently received her Ph.D. in Neuroscience from the University of Rochester School of Medicine, and was inducted as an alumni member of Nu Rho Psi.
Ron Saul, "Chronic activation of the substantia nigra nociceptin/orphanin receptor induces motor deficits similar to Parkinson's disease," 2008. Saul, the 2008 winner of the Neuroscience Award, infused a drug into the substantia nigra of rats and measured the resulting motor behaviors, mood disturbances, and cognitive abilities.
Romano, Alison (2012). Modeling disorders with the DIVA model : ataxic dysarthria. (Mentor: A. Jamieson)
This study examined the efficacy of the “directions into velocities of articulators” (DIVA) model, a neurologically plausible [artificial neural network] model of speech production, for studying a motor speech disorder known as “ataxic dysarthria”. Utilizing similar lesioning paradigms as used for DIVA models of stuttering and child deviations from adult speech, we set the connection weights of the critical neurological areas - the cerebellum and its cortical connections - to zero. Three lesions were made: one full cerebellar lesion, one lesion that destroyed the cerebellar neurons used to control auditory timing, and one lesion that destroyed the cerebellar neurons used to control somatosensory timing. The intact model and each of the lesioned models were taught five speech productions, which were recorded and compared based on formant analyses, pitch analysis, and voice analyses. Many of the productions were found to be differentially and significantly affected by the three lesions on many of the acoustic analyses (p<0.001 for many comparisons). Even though the lesions did not display the exact impairments as would be expected from a dysarthric speaker, it seems promising that by creating a lesion that combines elements of the auditory and somatosensory cerebellar lesions, we may be able to more accurately model ataxic dysarthria. With the proposed changes to the model, as well as the proposed future work, this line of research has many implications for modeling, understanding, and eventually treating ataxic dysarthria.